Significant improvements in animal performance, efficiency and carcass and meat quality have been made over the years through the application of standard animal breeding and selection techniques. However, such classical animal breeding techniques require several years of genetic evaluation of performance records on individual animals and their relatives and are therefore very expensive. Other efforts have been made to improve productivity and quality through the application of such management practices as the use of feed additives, animal hormonal implants and chemotherapeutics. However, there is significant political and regulatory resistance to the introduction and use of such methodologies. Such methodologies are also non-inheritable and need to be applied differently in every production system.
There is a need for methods that allow relatively easy and more efficient selection and breeding of farm animals with an advantage for an inheritable trait of circulating leptin levels, feed intake, growth rate, body weight, carcass merit and carcass composition. The economic significance of the use of genetic markers that are associated with specific economically important traits (especially traits with low heritability) in livestock through marker-assisted selection cannot therefore be over-emphasized.
The physiological regulation of intake, growth and energy partitioning in animals is under the control of multiple genes, which may be important candidates for unraveling the genetic variation in economically relevant traits (ERT) in beef production. Polymorphisms in these candidate genes that show association with specific ERT are useful quantitative trait nucleotides for marker-assisted selection
Mitochondrial transcription factor A (“TFAM”), a member of a high mobility group protein family and the first-identified mitochondrial transcription factor (Fisher and Clayton, Mol Cell Biol. 1988; 8:3496-509), is essential for maintenance and biogenesis of mitochondrial DNA (mtDNA). First, TFAM plays a histone-like role in mitochondria, as it is tightly associated with mtDNA as a main component of the nucleoid (Kanki et al. Mol Cell Biol. 2004; 24:9823-34). Evidence has shown that one molecule of mtDNA is packed with ˜900 molecules of TFAM on average (Alam et al. Nucleic Acids Res. 2003; 31:1640-5), which makes mtDNA no longer naked. Second, TFAM regulates mtDNA copy number in mammals. Investigation using a combination of mice with TFAM overexpression and TFAM knockout demonstrated that mtDNA copy number is directly proportional to the total TFAM protein level in mouse embryos (Ekstrand et al. Hum Mol Genet. 2004; 13:935-44). RNA interference of the endogenous TFAM expression in HeLa cells also indicated that the mtDNA amount is correlated in parallel with the amount of TFAM (Kanki et al. Ann N Y Acad Sci. 2004; 1011:61-8). Third, TFAM stimulates transcription of mtDNA. The TFAM protein possesses two tandem high mobility group domains, which makes TFAM bind, unwind and bend DNA without sequence specificity and thus facilitate transcription initiation of mtDNA (Gaspari et al. 2004; 1659:148-52). Evidence has shown that import of wt-TFAM into liver mitochondria from hypothyroid rats increased RNA synthesis significantly up to 4-fold (Garstka et al. Nucleic Acids Res. 2003; 31:5039-47).
It has been known for many years that adipose tissue plays a central rule in regulation and manipulation of energy metabolisms through the storage and turnover of triglycerides and through the secretion of factors that affect satiety and fuel utilization. However, many key aspects of adipogenesis are accompanied by stimulation of mitochondrial biogenesis (Wilson-Fritch et al. Mol Cell Biol. 2003; 23:1085-94). For example, the major site of fatty acid β-oxidation occurs in mitochondria (Reichert and Neupert, Trends Genet. 2004; 20:555-62), which may provide key intermediates for the synthesis of triglycerides via the action of pyruvate carboxylase (Owen et al. J Biol Chem. 2002; 277:30409-12). In addition, a relatively large mitochondrial mass are needed to generate acetyl-CoA for fatty acid activation prior to esterification into triglycerides. All these studies demonstrated the essential role and function of mitochondria in lipid metabolism.
To further explore the mechanism of mitochondria involved in adipogenesis, Wilson-Fritch and colleagues (Wilson-Fritch et al. Mol Cell Biol. 2003; 23:1085-94 and Wilson-Fritch et al. J Clin Invest. 2004; 114:1281-9) studied the 3T3-L1 cell (representative of white adipocytes) differentiation by using both proteomic and genomic approaches. Proteomic analysis revealed a 20- to 30-fold increase in the concentration of numerous mitochondrial proteins, while genomic analysis with gene expression profiling using Affymetrix GeneChips detected a statistically significant increase in the expression of many nucleus-encoded mitochondrial genes during adipogenesis. In particular, the authors found a profound decrease of approximately 50% in the levels of transcripts for nuclear-encoded mitochondrial genes accompanying the onset of obesity (Wilson-Fritch et al. J Clin Invest. 2004; 114:1281-9).
It remains advantageous to provide further SNPs that may more accurately predict the meat quality phenotype of an animal and also a business method that provides for increased production efficiencies in livestock cattle, as well as providing access to various records of the animals and allows comparisons with expected or desired goals with regard to the quality and quantity of animals produced.
Citation or identification of any document in this application is not an admission that such document is available as prior art to the present invention.